tbuckley/cabot-search huggingface dataset:
193P Differences in response to immunotherapy between KRAS G12C and KRAS non-G12C mutated NSCLC
Authors: L. Masfarre Pinto, P. Rocha, S. Clave, N. Navarro Gorro, I. Sanchez, M. Giner, A. Corbera Lloret, A. Taus Garcia, A.S.D.F.M. Parreira, B. Bellosillo Paricio, E. Arriola
Journal: Journal of Thoracic Oncology (2023)
Recommendations on diagnosis and antimicrobial treatment of infections after anterior cruciate ligament reconstruction (ACL-R) endorsed by ESSKA and EBJIS
Authors: Nora Renz, Tomislav Madjarevic, Matteo Ferrari, Roland Becker, Christen Ravn, Charles Vogely, Daniel Pérez-Prieto
Journal: Journal of Infection (2023)

Infection after anterior cruciate ligament reconstruction (ACL-R) is a rare but devastating complication affecting predominantly young and sportive individuals. A timely and correct diagnosis as well as optimized management is paramount to circumvent serious sequelae and compromise in life quality. These recommendations are primarily intended for use by infectious disease specialists and microbiologists, but also orthopedic surgeons and other healthcare professionals who care for patients with infections after ACL-R. They are based on evidence mainly originating from observational studies and opinions of experts in the field, and cover the management of infections after ACL-R with a special focus on etiology, diagnosis, antimicrobial treatment and prevention. Comprehensive recommendations on surgical treatment and rehabilitation are presented separately in a document primarily addressing orthopedic professionals.
10 Osimertinib versus gefitinib followed by osimertinib in patients with EGFR-mutant non-small cell lung cancer (NSCLC): EORTC Lung Cancer Group 1613 APPLE trial
Authors: J. Remon Masip, B. Besse, S. Ponce Aix, A. Callejo Perez, K. Al-Rabi, R. Bernabe Caro, L. Greillier, M. Majem Tarruella, N. Reguart Aransay, I. Monnet, S. Cousin, P. Garrido Lopez, G. Robinet, R. García Campelo, A-C. Madroszyk Flandin, J. Mazieres, H. Curcio, Y. Pretzenbacher, A-M.C. Dingemans, R. Dziadziuszko
Journal: Journal of Thoracic Oncology (2023)
136P Germline testing in a cohort of malignant mesothelioma (G-MESO)
Authors: E. Nadal, M. Gausachs, C. Castillo, A. Teulé, J. Brenes, M. Jové, R. Palmero, M. Mosteiro, S. Padrones, J. Bosch-Barrera, M. Pineda, E. Tornero, A. Alay, A. Lopez-Doriga, I. Brao, M. Arellano, J. Brunet, C. Lazaro
Journal: Journal of Thoracic Oncology (2023)
123P Second progression-free survival (PFS2) after first progression in patients receiving PACIFIC regimen: An exploratory analysis of the Blue Sky observational study
Authors: A.R.R. Filippi, J. Saddi, F. Agustoni, G. Galli, S. La Mattina, G. Facheris, S. Arcangeli, D.L. Cortinovis, G. Piperno, M.A. Zerella, A.G. Becchetti, L. Falcinelli, G. Stella, C. Bortolotto, A. Ferrari, P. Pedrazzoli, L. Preda, P. Borghetti
Journal: Journal of Thoracic Oncology (2023)
22P Adding anlotinib in gradual or local progression on first-line EGFR-TKIs for advanced non-small cell lung cancer: A single-arm, multicenter, phase II trial
Authors: H. Chen, Y. Hu, Y. Fan, G. Wu, S. Cang, Y. Yang, N. Yang, R. Ma, G. Jing, A. Liu, X. Xu, S. Tang, Y. Cheng, Y. Yu, Y-L. Wu
Journal: Journal of Thoracic Oncology (2023)
97P Aumolertinib as adjuvant therapy in postoperative EGFR-mutated stage I–III non-small cell lung cancer with high-risk pathological factors
Authors: X. Chen, J. He, H. Shen, Y. Xi, B. Chen, X. He, J. Gao, H. Yu, W. Shen
Journal: Journal of Thoracic Oncology (2023)
64P Pretreatment predictive score for metastatic non-small cell lung cancer patients treated with immunotherapy
Authors: A. Musaelyan, F. Moiseyenko, T. Emileva, A.P. Oganesyan, M. Urtenova, S. Odintsova, I. Chistyakov, A. Akopov, S. Orlov
Journal: Journal of Thoracic Oncology (2023)
24P Efficacy and safety of 1st generation EGFR TKI retreatment in EGFR mutation-positive, T790M-negative patients previously treated with 1st or 2nd generation EGFR TKI and cytotoxic chemotherapy
Authors: S.Y. Lee, J. Choi, J.C. Lee, C.M. Choi, I.A. Kim, K.Y. Lee, J.E. Lee, S.H. Jang, S.H. Yoon, I-J. Oh, S.H. Lee, E.Y. Kim
Journal: Journal of Thoracic Oncology (2023)
63P Inflammatory indexes and treatment response as correlates of pembrolizumab effectiveness in patients with PD-L1≥50%: Data from the real-life practice
Authors: M. Knetki-Wroblewska, S. Tabor, A. Płtużański, K. Winiarczyk, P. Sobczuk, Z. Lewandowska, A. Piórek, K. Zajda, A. Janowicz-Zebrowska, M. Zaborowska-Szmit, P. Badurak, M. Borucka, D.M. Kowalski, M. Krzakowski
Journal: Journal of Thoracic Oncology (2023)
218P Implications of the eighth edition of TNM staging system for thymoma, a single-center retrospective study
Authors: I. Vardi, D. Halperin, O. Ben David Ohayone, A. Stemmer, S. Sagie, D. Urban, S. Appel, H. Gantz Sorotsky, E. Marom, J. Bar
Journal: Journal of Thoracic Oncology (2023)
90P Cell-free DNA as a predictive and prognostic marker in adjuvant-treated non-small cell lung cancer
Authors: E. Azkona, R. Casas, J. Aurrekoetxea, I. De Elejoste Echebarria, M. Fernandez, J. Azcuna Sagarduy, L. García, M. Saiz, B. Ortega Gallastegi, B. Calvo
Journal: Journal of Thoracic Oncology (2023)
10MO EMPOWER-Lung 1: Cemiplimab (CEMI) monotherapy as first-line (1L) treatment of patients (pts) with brain metastases from advanced non-small cell lung cancer (aNSCLC) with programmed cell death-ligand 1 (PD-L1) ≥50% — 3-year update
Authors: S. Kilickap, M. Özgüroğlu, A. Sezer, M. Gumus, I. Bondarenko, M. Gogishvili, H.M. Türk, I. Cicin, D. Bentsion, O.A. Gladkov, P. Clingan, V. Sriuranpong, X. He, J-F. Pouliot, F. Seebach, I. Lowy, G. Gullo, P. Rietschel
Journal: Journal of Thoracic Oncology (2023)
70P Impact of TP53/KRAS mutations on overall survival of metastatic non-small cell lung cancer patients (pts) treated with systemic first-line therapy
Authors: S. Rubio Novella, A. Cobo, A. Montes, J. Soler Lopez, M. Arnal Rondan, S. Noguera Palanca, I. Tena, J. Miguel, B. Navarro, I. Domingo, S. Cases Esteban, M. Díaz, P. Andrade, E. Rosello, J.R. Lazaro Santander, D. Lorente Estelles, A. Sánchez Hernández
Journal: Journal of Thoracic Oncology (2023)
144P Exposure-lag response of surface net solar radiation on lung cancer incidence: A worldwide interdisciplinary and time-series study
Authors: X. Lu, R. Wang, J. Li, S. Lyu, J. Zhang, Q. Wang, W. Chi, R. Zhong, C. Chen, X. Wu, R. Hu, Z. You, Y. Mai, S. Xie, J. Lin, B. Zheng, Q. Zhong, J. He, W. Liang
Journal: Journal of Thoracic Oncology (2023)
50 Cemiplimab plus chemotherapy versus chemotherapy alone in non-small cell lung cancer: Longer follow-up results from the phase III EMPOWER-Lung 3 trial
Authors: T. Makharadze, M. Gogishvili, T. Melkadze, A. Baramidze, D. Giorgadze, K.D. Penkov, K. Laktionov, G. Nemsadze, M. Nechaeva, I. Rozhkova, E. Kalinka, S. Li, Y. Li, M. Kaul, J-F. Pouliot, F. Seebach, I. Lowy, G. Gullo, P. Rietschel
Journal: Journal of Thoracic Oncology (2023)
65P Correlation of overall survival and surrogate endpoints in advanced non-small cell lung cancer treated with immune checkpoint inhibitors: A trial-level analysis
Authors: F. Salomone, F. Napolitano, A. Caltavituro, R. Buonaiuto, G. Pecoraro, M.C. Isernia, A. Santaniello, L. Formisano, R. Bianco, A. Servetto
Journal: Journal of Thoracic Oncology (2023)
30 Long-term efficacy, safety, and predictors of response to amivantamab among patients with post-platinum EGFR Ex20ins-mutated advanced NSCLC
Authors: P. Garrido Lopez, N. Girard, B.C. Cho, J. Sabari, A. Spira, R.E. Sanborn, K. Goto, J.C-H. Yang, J. Curtin, X. Lyu, A. He, J. Penton, J. Edwards, G. Low Massin, K. Xia, M. Chioda, M. Thayu, R.E. Knoblauch, P. Mahadevia, N. Leighl
Journal: Journal of Thoracic Oncology (2023)
27P Amivantamab versus alternative real-world anti-cancer therapies in patients with advanced non-small cell lung cancer with epidermal growth factor receptor exon 20 insertion mutations in the US and Europe
Authors: N. Girard, J. Wolf, T.M. Kim, N. Leighl, C. Knott, T. Li, J. Cabrieto, J. Diels, J. Sermon, P. Mahadevia, C.A. Schioppa, J. Sabari
Journal: Journal of Thoracic Oncology (2023)
111P Application of radiomics signatures and unidimensional vs volumetric measurement of early tumor growth dynamics (TGD) to predict first-line treatment outcomes in patients with stage IV non-small cell lung cancer (NSCLC)
Authors: L. Schwartz, K. Aggarwal, D.J. Grootendorst, S. Kotapati, M. Fronheiser, B. Zhao, C. Coronado-Erdmann, M. Micsinai-Balan, M. Karasarides, A.T. Fojo, K. Brown
Journal: Journal of Thoracic Oncology (2023)
178P Targeting XPO1-dependent nuclear export of HMGB1 in non-small cell lung cancer
Authors: M. Gonzalez-Cao, X. Cai, J.W.P. Bracht, X. Han, Y. Yang, C. Pedraz, M.T. Moran Bueno, J. García-Corbacho, A. Aguilar, R. Bernabe Caro, P.R. De Marchi, L. Sussuchi Da Silva, L. Ferro Leal, R.M. Reis, J. Codony-Servat, E. Jantus Lewintre, M.A. Molina-Vila, P. Cao, R. Rosell
Journal: Journal of Thoracic Oncology (2023)
48P Characteristics and treatment patterns of patients with advanced or metastatic non-small cell lung cancer managed with first-line immuno-oncology strategies in Greece: Interim results of a real-world prospective study (IO-HORIZON)
Authors: H. Linardou, A. Charpidou, A. Koumarianou, G. Mountzios, P.A. Kosmidis, C. Christodoulou, D. Mavroudis, A.N. Christopoulou, I. Korantzis, S. Baka, M. Vaslamatzis, I. Athanasiadis, A. Koutras, D. Mauri, A. Kotsakis, D. Ziogas, A. Desiniotis, I. Dimitriadis, K. Syrigos
Journal: Journal of Thoracic Oncology (2023)
72P Association of receptor activator of nuclear factor kappa-B ligand (RANKL) and epidermal growth factor receptor (EGFR) gene expression with bone metastases (mets) in patients (pts) with metastatic non-small cell lung cancer (mNSCLC)
Authors: A. Brouns, L. Hendriks, I. Robbesom-van den Berge, A. Driessen, G. Roemen, B. van Herpen, Z. Dekkers, B. Heitzer, D. Leunissen, L. Moonen, R. Lunde, M. Westenend, M. van Driel, E-J.M. Speel, A-M.C. Dingemans
Journal: Journal of Thoracic Oncology (2023)
Abstract SY29-01: Integrating evolutionary dynamics into cancer therapy
Authors: Robert A. Gatenby
Journal: Cancer Research (2023)

Abstract Evolution of resistance remains a barrier to successful therapy in most metastatic cancers despite the increasing number of treatment options. A major driver of the evolutionary capacity of cancer populations is the dynamic interactions of spatial and temporal variations in environmental conditions with malignant cells that can access a vast number of phenotypic properties encoded in the human genome. The research paradigm in cancer treatment remains focused on finding “magic bullets” that can kill all cancer cells while leaving normal cells unharmed - the cure for cancer. Current standard of care principles for metastatic cancers applies one or more drugs as though they were the cure for cancer - continuously at Maximum Tolerated Dose (MTD) until unambiguous evidence of tumor progression. However, because of the phenotypic diversity in most large metastatic cancers, this approach is usually unsuccessful because continuous MTD therapy will eventually kill the population of drug-sensitive cells and leave behind a population of resistant cancer cells that can proliferate unopposed by competition with other populations. I will discuss integration of evolutionary dynamics into cancer therapy. Arguably, this is already widespread because the search for magic bullets and the MTD treatment strategy is built upon an implicit assumption that cancer cure requires a one-cause, one-event extinction similar to the KT impact that eradicated non-avian dinosaurs. However, investigations of recent actual (e.g., Passenger pigeons) and attempted (e.g., pest management) species extinctions in the Anthropocene era have demonstrate more complex dynamics. In fact, most species extinctions are caused by a sequence of perturbations none of which, by itself, could eradicate the population. These dynamics can be integrated into evolution-based treatment approaches to control and perhaps cure currently fatal metastatic cancers with currently available (i.e., non-magic bullet) drugs. Citation Format: Robert A. Gatenby. Integrating evolutionary dynamics into cancer therapy. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr SY29-01.
Abstract 5146: <i>In vitro</i> neutrophil assays to support immuno-oncology drug development
Authors: Alanah Pieters, Martijn Vlaming, Jezabel Lefevere, Sofie Pattyn
Journal: Cancer Research (2023)

Abstract Neutrophils have shown a lot of plasticity with important consequences on cancer disease progression and have been associated with multiple functions such as killing antibody-opsonized cancer cells, directly kill tumor cells through the release of reactive oxygen and nitrogen species and a controversial role in the tumor micro-environment with both pro- and anti-tumor roles. Studying neutrophil function in vitro can be done using the Incucyte® live imaging system to monitor antibody-dependent cell-mediated cytotoxicity (ADCC). Optimised in vitro assays using fresh human neutrophils and fluorescent-labeled tumor cells can be used to screen the potency of candidate therapeutics. Additionally, neutrophil chemotaxis can be monitored using transwell plates and live imaging via Incucyte®. Finally, multiplex cytokine and chemokine analysis after activation and stimulation of neutrophils can be evaluated using Luminex technology. When studying neutrophil activity in vitro, important factors such as access to fresh blood and optimized protocols for purifying untouched neutrophils are key for reproducible and reliable results. Citation Format: Alanah Pieters, Martijn Vlaming, Jezabel Lefevere, Sofie Pattyn. In vitro neutrophil assays to support immuno-oncology drug development. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 5146.
Abstract 6588: Systems biology-based drug repositioning and biomarker discovery for Thai liver fluke-associated cholangiocarcinoma
Authors: Supawan Jamnongsong, Patipark Kueanjinda, Piyathida Tawornparcha, Kulthida Vaeteewoottacharn, Seiji Okada, Siwanon Jirawatnotai, Ananya Pongpaibul, Krittiya Korphaisarn, Somponnat Sampattavanich
Journal: Cancer Research (2023)

Abstract Our group has recently reported the successful use of comprehensive drug response and pan-omic profiling for identifying repurposable drug shortlists in Asian cholangiocarcinoma. We also developed the CCA45 gene-expression signature that could accurately predict the prognosis of CCA patients, especially those with Asian ethnic backgrounds. To further explore therapeutic candidates and potential resistance mechanisms, we have established CCA1 cell lines resistant to their subgroup-specific drug candidates: MEK and SRC inhibitors. Reverse-phase protein arrays (RPPA)-based proteomic profiling revealed upregulation of cell cycle, apoptosis, MAPK, and mTOR-related proteins in both MEKi- and SRCi-resistant cells. Src pathway activity was found to be more significantly reduced in SRCi-resistant cells. We identified CDK4/6 inhibitors as the second-line therapeutic candidates for MEK inhibitor-resistant cells by systematic drug screening. SRCi-resistant cells unexpectedly developed cross-resistance to MEK inhibitors and showed sensitivity to only a few CDK4/6 inhibitors. These data are beneficial for the clinical translation of our proposed drug candidates for Asian CCA, preparing the alternate regimens after drug resistance. We also adopted the DSP-based spatial transcriptomic platform to compare the tumor microenvironment between chemotherapy-sensitive and chemotherapy-resistant CCA patients. While the CTA panel showed consistent patterns of normalized gene expression to those of the WTA panel, the CTA panel can only measure 17 of the 45 genes required for our CCA45 signature. Out of these 17 genes, ITGB4, FGFR3, VEGFC, NOTCH1, and RRAD showed significant gene expression changes with reducing tumor percentage. The microenvironment of gemcitabine/cisplatin responder (R) non-responder (NR) exhibited negative regulation of ERK1/2 and MAPK, high WNT pathway activity, and high tumor-infiltrating lymphocyte (TIL). In contrast, the microenvironment of the non-responder (NR) subgroup showed high neutrophil-related activity, high NFκB, high Treg, and the exhausted immune phenotype. Overall, our study contributes toward realizing the precision medicine concept for CCA patients. Citation Format: Supawan Jamnongsong, Patipark Kueanjinda, Piyathida Tawornparcha, Kulthida Vaeteewoottacharn, Seiji Okada, Siwanon Jirawatnotai, Ananya Pongpaibul, Krittiya Korphaisarn, Somponnat Sampattavanich. Systems biology-based drug repositioning and biomarker discovery for Thai liver fluke-associated cholangiocarcinoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 6588.
Abstract 268: Antitumor CD4+ T cells reprogram tumor metabolism to drive progressive tumor regression
Authors: Caitlin Brandle, Ogacheko D. Okoko, Md Yeashin Gazi, Xin Wang, Mercy Kehinde-Ige, Huidong Shi, Gang Zhou
Journal: Cancer Research (2023)

Abstract Adoptive cell therapy has revolutionized the landscape of cancer immunotherapy, exhibiting unprecedented success in treating various types of cancer. Substantial investigative efforts have been devoted to gaining a deeper understanding of the ways in which adoptively transferred T cells eliminate tumors and to discovering strategies that enhance T cell functionality in the tumor microenvironment. We have established an experimental mouse model in which adoptive transfer of tumor-specific CD4+ T cells leads to eradication of established tumors. Using this model, we previously reported on the profound disruption of tumor metabolism induced by adoptive T cell therapy. However, the detailed mechanisms that enable tumor-reactive CD4+ T cells to alter tumor metabolism remain largely undefined. In the current study, we aimed to identify the key metabolic enzymes and pathways targeted by antitumor CD4+ T cells that lead to progressive tumor regression. Utilizing next-generation sequencing strategies, including bulk and single-cell RNA sequencing, we examined the metabolic changes cancer cells undergo in response to treatment, and the immune cell compositions in the tumor microenvironment. Additionally, we performed an in vivo CRISPR knockout screen to identify the metabolic genes that either sensitize tumor cells to adoptive cell therapy or contribute to tumor resistance. Results from our study may also illuminate potential targets in cancer metabolism that can be exploited using small-molecule inhibitors when adoptive cell therapy is not feasible. Citation Format: Caitlin Brandle, Ogacheko D. Okoko, Md Yeashin Gazi, Xin Wang, Mercy Kehinde-Ige, Huidong Shi, Gang Zhou. Antitumor CD4+ T cells reprogram tumor metabolism to drive progressive tumor regression [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 268.
Abstract 346: Downregulating KIF4A inhibited growth of uterine leiomyosarcoma by regulating cell cycle
Authors: Satoshi Nakagawa, Chihiro Mizuta-Odani, Mariya Kobayashi, Mamoru Kakuda, Kosuke Hiramatsu, Toshihiro Kimura, Eiji Kobayashi, Yutaka Ueda, Tadashi Kimura
Journal: Cancer Research (2023)

Abstract [Objective] Uterine leiomyosarcoma (LMS) has a poor prognosis, and no effective treatment other than surgery has been established. Kinesin family member4A (KIF4A) is a member of the kinesin4 subfamily and plays an important role in cell division. KIF4A has been revealed to play significant roles in some cancers with tumor proliferation. The aim of this study is to clarify the relationship between KIF4A and tumor growth of LMS. [Methods] One normal human uterine smooth muscle cell line and three LMS cell lines(SK-UT1, SK-LMS and SKN) were used to identify tumor-specific elevated proteins with iTRAQ(isobaric tags for relative and absolute quantitation). SiRNA and ShRNA were used to downregulate KIF4A in vitro and in in vivo. Cell variability was evaluated by MST-8 assay. Cell cycle analysis by fluorescence-activated cell sorting (FACS) and western blotting (WB) were performed to analyze the signal pathway. Immunostaining of 26 clinical specimen from patients operated at our university hospital since 1999 to 2021. [Results] A total of 2084 proteins were identified by iTRAQ. KIF4A was identified as a protein with more than twice the expression level of normal smooth muscle cells. WB confirmed high expression of KIF4A in all three LMS cell lines. And in immunostaining of clinical specimens, KIF4A was positive in 20/26(76.9%) cases. A trend toward worse prognosis was suggested in the group with high KIF4A expression (no significant difference due to the small number of cases). Downregulation with SiRNA significantly suppressed the growth of LMS cell lines in vitro (-37.2±4.73% in SK-LMS, -87.7±4.02% in SKN and -28.1±3.00% in SK-UT1, p&amp;lt;0.05). By FACS, G2/M phase cells was significantly increased in KIF4A suppressed cell lines and by WB, p-cdc2 was upregulated in KIF4A suppressed cells. In vivo, downregulation of KIF4A was found to significantly suppress tumor size in genograft mice. (1186±118mm³ vs 461±84mm³ in SK-LMS and 1704±441mm³ vs 514±230mm³ in SK-UT1, p&amp;lt;0.05, f). [Conclusion] Downregulating KIF4A inhibited LMS tumor growth and it can be a novel therapeutics target to treat LMS. Citation Format: Satoshi Nakagawa, Chihiro Mizuta-Odani, Mariya Kobayashi, Mamoru Kakuda, Kosuke Hiramatsu, Toshihiro Kimura, Eiji Kobayashi, Yutaka Ueda, Tadashi Kimura. Downregulating KIF4A inhibited growth of uterine leiomyosarcoma by regulating cell cycle [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 346.